By a News Reporter-Staff News Editor at Gene Therapy Weekly -- Investigators publish new report on Ischemia. According to news reporting originating from Jiangsu, People's Republic of China, by NewsRx correspondents, research stated, "Global cerebral ischemia/reperfusion (I/R) facilitates the activation of procaspase-3 and promotes apoptosis in hippocampus. But the mechanisms have remained uncharacterized."
Our news editors obtained a quote from the research from Xuzhou Medical College, "Protein S-nitrosylation and denitrosylation is an important reversible posttranslational modification, which is a common mechanism in signal transduction and affects numerous physiological and pathophysiological events. However, it is not known whether S-nitrosylation/denitrosylation modification of procaspase-3 serves as a component of apoptosis and cell death induced by cerebral I/R. Here we show that procaspase-3 is significantly denitrosylated and activated after I/R in rat hippocampus. NS102, a glutamate receptor 6 (GluR6) antagonist, can inhibit the denitrosylation of procaspase-3 and diminish the increased Fas ligand (FasL) and thioredoxin (Trx)-2 expression induced by cerebral I/R. Moreover, downregulation of FasL expression by antisense oligodeoxynucleotides inhibits the denitrosylation and activation of procaspase-3. Auranofin, a TrxR inhibitor or TrxR2 antisense oligodeoxynucleotide, has similar effects. In primary hippocampal cultures, Lentiviral-mediated knockdown of FasL and TrxR2 before the oxygen and glucose deprivation/reoxygenation further verifies that FasL and TrxR2 are involved in the denitrosylation of procaspase-3. In situ TUNEL staining and cresyl violet staining validate that inhibiting denitrosylation of procaspase-3 may exert neuroprotective effect on apoptosis and cell death induced by cerebral I/R in hippocampal CA1 pyramidal neurons."
According to the news editors, the research concluded: "This is the first evidence that cerebral I/R mediates procaspase-3 denitrosylation and activation through GluR6-FasL-Trx2 pathway, which leads to neuronal apoptosis and cell death."
For more information on this research see: GluR6-FasL-Trx2 mediates denitrosylation and activation of procaspase-3 in cerebral ischemia/reperfusion in rats. Cell Death & Disease, 2013;4():274-284. Cell Death & Disease can be contacted at: Nature Publishing Group, Macmillan Building, 4 Crinan St, London N1 9XW, England. (Nature Publishing Group - www.nature.com/; Cell Death & Disease - www.nature.com/cddis/)
The news editors report that additional information may be obtained by contacting N. Sun, Xuzhou Medical College, Res Center Biochem & Mol Biol, Jiangsu Key Lab Brain Dis Bioinformat, Xuzhou 221004, Jiangsu, People's Republic of China. Additional authors for this research include J.R. Hao, X.Y. Li, X.H. Yin, Y.Y. Zong, G.Y. Zhang and C. Gao (see also Ischemia).
Keywords for this news article include: Asia, Antisense Technology, Biotechnology, Jiangsu, Apoptosis, Reperfusion, Bioengineering, Brain Ischemia, Medical Devices, Blood Transfusion, Transfusion Medicine, People's Republic of China
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